Bone marrow stromal cells (BMSCs) have shown significant promise in the treatment of disease, but their therapeutic efficacy is often limited by inefficient homing of systemically administered cells, which results in low number of cells accumulating at sites of pathology. BMSC home to areas of inflammation where local expression of cell adhesion molecules and chemokine gradients are present. Pulsed FUS (pFUS) employs non-continuous exposures, that lower the rate of energy deposition and allow cooling to occur between pulses, thereby minimizing thermal effects and emphasizing the effects created by non-thermal mechanisms of FUS (i.e. acoustic radiation forces and acoustic cavitation). We examined changes in muscle and kidney following pFUS has little effect on the histological integrity of the tissue and does not induce cell death. pFUS increased expression of several chemoattractants creating a transient molecular zip code on days 0 and 1 following pFUS that returns to baseline levels by day 3 post-pFUS. pFUS exposures induced up-regulation of cell adhesion molecules on muscle vasculature. The observed molecular changes in muscle following pFUS may be utilized to target cellular therapies, by increasing homing to areas of pathology. We induce a mechanotransductive response that initiates a largely an anti-inflammatory M2-type macrophage environment. We demonstrated local upregulation of chemoattractants in pFUS-treated skeletal muscle and kidney leads to enhance homing, permeability, and retention of BMSC or human endothelial precursor cells (EPC). Furthermore, the magnitude of BMSC or EPC homing was increased when pFUS treatments and cell infusions were repeated daily in muscle. We also demonstrate that the induced molecular changes following pFUS to muscle and kidney can be block by ibuprofen, a cyclooxygenase 2 inhibitor, or TNF alpha receptor binding protein, etanercept, indicating that the mechanotransductive effects are acting through a COX 2 pathway in the tissue. Both ibuprofen or etanercept administered prior to pFUS and stem cell infusion block the homing of stem cells to targeted muscle which indicated that using this approach we can use pFUS to interrogate drug-host tissue interactions and their effect on homing. We also demonstrated that pFUS exposures in combination with BMSC in an acute kidney injury model induce mechanotransductive effects in the murine kidney (AKI). To examine the efficacy of pFUS-enhanced cell homing in disease, we targeted pFUS to kidneys to enhance BMSC homing after cisplatin-induced AKI. We found that pFUS enhanced BMSC homing at 1 day post-cisplatin, prior to renal functional deficits, and that enhanced homing improved outcomes of renal function, tubular cell death, and regeneration at 5 days post-cisplatin compared to BMSCs alone. After observing improved homing and AKI outcomes during early AKI, we investigated whether pFUS+BMSC therapy could rescue established AKI. BMSC administration alone at 3 days post-cisplatin, after renal functional deficits become obvious, significantly improved 7-day survival of animals. Survival was further improved using pFUS+BMSC. BMSCs, alone or with pFUS, shifted the kidney macrophage phenotype from M1 to M2. This study shows that pFUS serves as a neoadjuvant treatment to improve MSC homing to diseased organs. pFUS coupled with BMSCs enhances cellular therapy to prevent AKI and allows rescue therapy in established AKI, which currently has no meaningful therapeutic options.